Benign Prostatic Hyperplasia (BPH) is a common disorder characterized by the enlargement of the prostate gland over a prolonged period of time. Benign hyperplasia of the prostate develops in men around the age of 40-45 and slowly progresses until death (McCance & Huether, 2014).
The actual pathophysiology of BPH and how it develops is complex and focuses on the following:
1. Levels and ratios of endocrine factors such as (McCance & Huether, 2014):
- Androgens
- Estrogens
- Gonadotropins
- Prolactin
2. Alterations in the balance of autocrine/paracrine growth-stimulatory and growth inhibitory factors such as (McCance & Huether, 2014):
- Insulin-like growth factors (IGFs)
- Epidermal growth factor
- Nerve growth factor
- Fibroblast factors
- IGF binding proteins
- Transforming growth factor-beta (TGF-β)
Aging along with circulating androgens, have potential to disrupt the balance of growth factor signaling pathways and stromal/epithelial interactions creating a growth-promoting and tissue remodeling microenvironment. This process can contribute to prostatic enlargement and the development of BPH (McCance & Huether, 2014).
Testosterone is the primary circulating androgen in men. Testosterone has the potential to be metabolized through CYP19/aromatase into the potent estrogen, estradiaol-17β. The prostate is an estrogen target tissue and estrogens can affect the growth and differentiation of the prostate. Estrogens along with selective estrogen receptor modulators have been shown to impact prostate proliferation demonstrating a potential role in the development of BPH (McCance & Huether, 2014).
These interactions and changes that occur can lead to an increase in prostate volume by:
Local inflammation within the remodeled stroma which occurs with altered cytokine, reactive oxygen/nitrogen species, and chemoattractants. This results in increased oxygen demands of proliferating cells causing local hypoxia that promotes angiogenesis and changes to fibroblasts. Functional and phenotypic changes (transdifferentiation) of fibroblasts to the myofibroblasts is the main feature of the remodeled microenvironment (McCance & Huether, 2014).
BPH begins in the inner glands of the prostate known as the periurethral glands. The prostate then becomes enlarged as nodules form and grow (nodular hyperplasia) and glandular cells enlarge and become hypertrophied (McCance & Huether, 2014).
As hyperplasia of the prostatic tissue progresses it can cause bladder outflow obstruction and lower urinary tract symptoms (LUTS) such as (McCance & Huether, 2014):
- Increased urinary urgency
- Delay in starting urination
- Decreased force in urinary stream
As urethral obstruction progresses secondary to BPH the male may have difficulty completely emptying the bladder leading to urinary retention.
Prolonged urinary retention can lead to (McCance & Huether, 2014):
- Increase in intra-abdominal pressure
- Significantly decreased force in urinary stream
- Increased length of time to initiate and complete voiding
- Hematuria, bladder or kidney infections, hydroureter, hydronephrosis, and renal insufficiency
Approximately one half of all men who have a diagnosis of benign prostatic hyperplasia have moderate to severe lower urinary tract symptoms (LUTS) (American-Urology-Association, 2003).
(Solomon, 2015)
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